PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15205031-9 2004 Acute (24-h) silica exposure decreased AMs, increased PMNs, increased LDH activity and levels of albumin, TNF-alpha, and MIP-2 in BAL fluid, and enhanced AM-CL in both iNOS KO and WT mice. Silicon Dioxide 13-19 tumor necrosis factor Mus musculus 106-115 17007523-0 2006 Sensitive immunoassay of a biomarker tumor necrosis factor-alpha based on poly(guanine)-functionalized silica nanoparticle label. Silicon Dioxide 103-109 tumor necrosis factor Mus musculus 37-64 17007523-1 2006 A novel electrochemical immunosensor for the detection of tumor necrosis factor-alpha (TNF-alpha) based on poly(guanine)-functionalized silica nanoparticles (NPs) label is presented. Silicon Dioxide 136-142 tumor necrosis factor Mus musculus 58-85 17007523-1 2006 A novel electrochemical immunosensor for the detection of tumor necrosis factor-alpha (TNF-alpha) based on poly(guanine)-functionalized silica nanoparticles (NPs) label is presented. Silicon Dioxide 136-142 tumor necrosis factor Mus musculus 87-96 16333916-4 2005 Tumor necrosis factor (TNF)-alpha, inducible nitric oxide synthase (iNOS), interferon (IFN)-alpha, and interleukin-6 mRNAs were detected to a much greater extent in silica-treated mice compared with control mice after HSV-1 infection, and excessive expression of iNOS mRNA and cytokine mRNAs in the liver may be closely related to massive liver cell apoptosis. Silicon Dioxide 165-171 tumor necrosis factor Mus musculus 0-33 15849212-5 2005 The production of tumor necrosis factor-alpha in lavage fluid was significantly enhanced in CD204 null mice compared with wild-type mice following silica exposure. Silicon Dioxide 147-153 tumor necrosis factor Mus musculus 18-45 15261785-4 2004 Exposure of RAW 264.7 cells to aged silica particles induced macrophage activation (evidenced by the morphological features observed with scanning electron microscopy and by the release of TNF-alpha and IL-6) and impairment of phagocytosis of test particles, even at noncytotoxic doses. Silicon Dioxide 36-42 tumor necrosis factor Mus musculus 189-198 15204774-5 2004 The levels of tumor necrosis factor (TNF)-alpha were significantly increased (1.5-fold) in the bronchoalveolar lavage fluid of the silica-exposed mice as compared to the saline-exposed mice. Silicon Dioxide 131-137 tumor necrosis factor Mus musculus 14-47 15204774-9 2004 Therefore, the silica-induced alterations in immunoglobulin levels, increased TNF-alpha, increased B1a B cells and CD4+ T cells, with decreased regulatory T cells, may provide an environment that allows for increased autoreactivity. Silicon Dioxide 15-21 tumor necrosis factor Mus musculus 78-87 12500662-4 2002 RESULTS: Inhalation of silica increased the level of tumor necrosis factor-alpha (TNF-alpha), and of the 66 and 63 kDa peptides in the BAL fluid in comparison to sham-treated control. Silicon Dioxide 23-29 tumor necrosis factor Mus musculus 53-80 14570868-3 2004 Silica induction of apoptosis in macrophages might be mediated by TNFalpha. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 66-74 14570868-5 2004 Therefore, we studied the TNFalpha-mediated mechanisms that confer macrophage protection against the pro-apoptotic effects of silica. Silicon Dioxide 126-132 tumor necrosis factor Mus musculus 26-34 14570868-6 2004 We will show that exposure to silica induced TNFalpha production by RAW 264.7 cells, but not by IC-21. Silicon Dioxide 30-36 tumor necrosis factor Mus musculus 45-53 14570868-11 2004 Protection against apoptosis in RAW 264.7 cells in response to silica was mediated by enhanced NF-kappaB activation and ERK-mediated phosphorylation of the p55 TNFalpha receptor. Silicon Dioxide 63-69 tumor necrosis factor Mus musculus 160-168 12604844-1 2003 Previous studies suggest that tumor necrosis factor alpha (TNF-alpha) and the TNFRI (p55) and TNFRRII (p75) receptors mediate the pulmonary fibrotic response to silica. Silicon Dioxide 161-167 tumor necrosis factor Mus musculus 30-57 12604844-1 2003 Previous studies suggest that tumor necrosis factor alpha (TNF-alpha) and the TNFRI (p55) and TNFRRII (p75) receptors mediate the pulmonary fibrotic response to silica. Silicon Dioxide 161-167 tumor necrosis factor Mus musculus 59-68 12500662-4 2002 RESULTS: Inhalation of silica increased the level of tumor necrosis factor-alpha (TNF-alpha), and of the 66 and 63 kDa peptides in the BAL fluid in comparison to sham-treated control. Silicon Dioxide 23-29 tumor necrosis factor Mus musculus 82-91 12500662-5 2002 Pre-treatment of silica exposed mice with NAT leaf extract significantly prevented the accumulation of TNF-alpha in the BAL fluid, but the 66 and 63 kDa peptides remained unchanged. Silicon Dioxide 17-23 tumor necrosis factor Mus musculus 103-112 11457890-2 2001 Wild-type mice instilled with silica developed severe pulmonary inflammation, with local production of tumor necrosis factor (TNF)-alpha, and interstitial neutrophil and macrophage infiltration in the lungs. Silicon Dioxide 30-36 tumor necrosis factor Mus musculus 103-136 12091251-0 2002 Silica-induced apoptosis in murine macrophage: involvement of tumor necrosis factor-alpha and nuclear factor-kappaB activation. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 62-89 12091251-2 2002 Silica exposure induces tumor necrosis factor (TNF)-alpha release and nuclear factor (NF)-kappaB activation, and apoptotic mechanisms have been implicated in silica-induced pathogenesis. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 24-57 11850347-1 2002 Crystalline silica stimulates macrophages in vitro to release interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) and induces apoptosis of macrophages. Silicon Dioxide 12-18 tumor necrosis factor Mus musculus 92-119 11850347-1 2002 Crystalline silica stimulates macrophages in vitro to release interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide (NO) and induces apoptosis of macrophages. Silicon Dioxide 12-18 tumor necrosis factor Mus musculus 121-130 11208652-9 2001 All murine strains enhanced TNF and alpha1(I) collagen mRNA in response to silica. Silicon Dioxide 75-81 tumor necrosis factor Mus musculus 28-31 11208652-1 2001 Murine exposure to silica is associated with enhanced tumor necrosis factor alpha (TNF-alpha) expression and matrix deposition. Silicon Dioxide 19-25 tumor necrosis factor Mus musculus 54-81 10569191-0 1999 Dependence of NF-kappaB activation and free radical generation on silica-induced TNF-alpha production in macrophages. Silicon Dioxide 66-72 tumor necrosis factor Mus musculus 81-90 11208652-1 2001 Murine exposure to silica is associated with enhanced tumor necrosis factor alpha (TNF-alpha) expression and matrix deposition. Silicon Dioxide 19-25 tumor necrosis factor Mus musculus 83-92 11570673-7 2001 ICAM-1 expression on silica-exposed mouse macrophages is enhanced by reactive oxygen species (ROS) and tumor necrosis factor-alpha (TNF-alpha) and appears to be regulated through specific sequence elements within the ICAM-1 promoter. Silicon Dioxide 21-27 tumor necrosis factor Mus musculus 103-130 11570673-7 2001 ICAM-1 expression on silica-exposed mouse macrophages is enhanced by reactive oxygen species (ROS) and tumor necrosis factor-alpha (TNF-alpha) and appears to be regulated through specific sequence elements within the ICAM-1 promoter. Silicon Dioxide 21-27 tumor necrosis factor Mus musculus 132-141 26368622-6 2000 As an example, mice with the genes knocked out for both the 55- and 75-kD receptors for tumor necrosis factor-alpha (TNF-alpha) are protected from the fibrogenic effects of inhaled asbestos and silica. Silicon Dioxide 194-200 tumor necrosis factor Mus musculus 88-115 26368622-6 2000 As an example, mice with the genes knocked out for both the 55- and 75-kD receptors for tumor necrosis factor-alpha (TNF-alpha) are protected from the fibrogenic effects of inhaled asbestos and silica. Silicon Dioxide 194-200 tumor necrosis factor Mus musculus 117-126 10569191-2 1999 The present study investigates the role nuclear transcription factor kappaB (NF-kappaB) and oxygen free radicals in silica-induced TNFalpha production in primary alveolar macrophages and RAW 264.7 cells. Silicon Dioxide 116-122 tumor necrosis factor Mus musculus 131-139 10569191-3 1999 Using electrophoretic mobility shift assay (EMSA) and enzyme-linked immunoadsorbent assay (ELISA), we have demonstrated that silica can induce NF-kappaB activation and TNFalpha expression in a dose-dependent manner. Silicon Dioxide 125-131 tumor necrosis factor Mus musculus 168-176 10569191-5 1999 Inhibition of NF-kappaB activation by SN50, a specific NF-kappaB blocker, abolishes silica-induced TNFalpha production. Silicon Dioxide 84-90 tumor necrosis factor Mus musculus 99-107 10569191-7 1999 These results indicate that silica-mediated free radical generation and NF-kappaB activation play important roles in silica-induced TNFalpha gene expression. Silicon Dioxide 28-34 tumor necrosis factor Mus musculus 132-140 10569191-7 1999 These results indicate that silica-mediated free radical generation and NF-kappaB activation play important roles in silica-induced TNFalpha gene expression. Silicon Dioxide 117-123 tumor necrosis factor Mus musculus 132-140 10385602-0 1999 Soluble tumor necrosis factor (TNF) receptors p55 and p75 and interleukin-10 downregulate TNF-alpha activity during the lung response to silica particles in NMRI mice. Silicon Dioxide 137-143 tumor necrosis factor Mus musculus 90-99 10385602-1 1999 We have found reduced activity of tumor necrosis factor (TNF)-alpha accompanying resolving and fibrosing alveolitis induced in NMRI mice by mineral particles (MnO2 and SiO2, respectively), which is in apparent contradiction to the well-recognized proinflammatory and profibrotic activities of this cytokine. Silicon Dioxide 168-172 tumor necrosis factor Mus musculus 34-67 10385602-4 1999 The downregulation of the TNF-alpha protein was concurrent with the accumulation of recruited polymorphonuclear neutrophils (PMNs) in alveoli, and coculture experiments showed that PMN explanted from the lungs of mice treated with silica particles were able to downregulate the expression of TNF-alpha protein by naive alveolar macrophages. Silicon Dioxide 231-237 tumor necrosis factor Mus musculus 26-35 10385602-4 1999 The downregulation of the TNF-alpha protein was concurrent with the accumulation of recruited polymorphonuclear neutrophils (PMNs) in alveoli, and coculture experiments showed that PMN explanted from the lungs of mice treated with silica particles were able to downregulate the expression of TNF-alpha protein by naive alveolar macrophages. Silicon Dioxide 231-237 tumor necrosis factor Mus musculus 292-301 10385602-5 1999 In addition, PMN depletion prevented the downregulation of TNF-alpha induced by silica, further establishing the role of PMNs in the downregulation of TNF-alpha. Silicon Dioxide 80-86 tumor necrosis factor Mus musculus 59-68 10385602-5 1999 In addition, PMN depletion prevented the downregulation of TNF-alpha induced by silica, further establishing the role of PMNs in the downregulation of TNF-alpha. Silicon Dioxide 80-86 tumor necrosis factor Mus musculus 151-160 10362723-0 1999 Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-alpha-induced oxidant stress. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 77-86 10362723-3 1999 We hypothesize that non-oxidant-mediated silica-cell interactions lead to the upregulation of tumor necrosis factor-alpha (TNF-alpha), whereby TNF-alpha-induced generation of reactive oxygen species (ROS) leads to the activation of the monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-2 genes. Silicon Dioxide 41-47 tumor necrosis factor Mus musculus 94-121 10362723-3 1999 We hypothesize that non-oxidant-mediated silica-cell interactions lead to the upregulation of tumor necrosis factor-alpha (TNF-alpha), whereby TNF-alpha-induced generation of reactive oxygen species (ROS) leads to the activation of the monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-2 genes. Silicon Dioxide 41-47 tumor necrosis factor Mus musculus 123-132 10362723-3 1999 We hypothesize that non-oxidant-mediated silica-cell interactions lead to the upregulation of tumor necrosis factor-alpha (TNF-alpha), whereby TNF-alpha-induced generation of reactive oxygen species (ROS) leads to the activation of the monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-2 genes. Silicon Dioxide 41-47 tumor necrosis factor Mus musculus 143-152 10362723-8 1999 This ROS production could be inhibited with extracellular GSH treatment, and in the case of cristobalite-induced ROS, inhibition was also achieved with an anti-TNF-alpha antibody. Silicon Dioxide 92-104 tumor necrosis factor Mus musculus 160-169 10362723-9 1999 The results support the hypothesis that TNF-alpha mediates cristobalite-induced MCP-1 and MIP-2 expression through the generation of ROS. Silicon Dioxide 59-71 tumor necrosis factor Mus musculus 40-49 9843848-0 1998 Silica-induced chemokine expression in alveolar type II cells is mediated by TNF-alpha. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 77-86 10101016-4 1999 Silica induced increased (over saline-treated animals) expression of TNF mRNA in double TNFR knockout (Ko), C57BL/6, BALB/c, and 129/J mice. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 69-72 10101016-10 1999 Even though silica and bleomycin induced increases in TNF in the TNFR Ko mice, the mice were protected from the fibrogenic effects of these agents. Silicon Dioxide 12-18 tumor necrosis factor Mus musculus 54-57 10100728-3 1998 The immunohistochemical analysis of lung tissue sections after silica instillation demonstrated the increased alveolar and interstitial tissue expression of all surface antigens and cytokines studied, mainly Mac-1, F4/80 antigens, TNF-alpha and IL-1beta, which were occasionally observed in normal uninjected and saline-treated mice. Silicon Dioxide 63-69 tumor necrosis factor Mus musculus 231-240 10100728-4 1998 These findings show that, after silica instillation, the expression of surface phenotypical markers of lung macrophages increased, and this change was concomitantly associated with an increased expression of the cytokines TNF-alpha and IL-1beta. Silicon Dioxide 32-38 tumor necrosis factor Mus musculus 222-231 9551885-2 1998 In vivo depletion of NK cells by anti-asialoGM1 Ab or macrophage depletion by silicon dioxide treatment reduced abortion rates, which could no longer be boosted by injecting TNF-alpha (which activates NK cells) or IFN-gamma (which activates macrophages). Silicon Dioxide 78-93 tumor necrosis factor Mus musculus 174-183 9843848-10 1998 The results indicate that the cristobalite-induced chemokine response in the lung epithelium is mediated in part by TNF-alpha and can be enhanced by macrophage- and lymphocyte-derived inflammatory mediators in an additive and synergistic fashion. Silicon Dioxide 30-42 tumor necrosis factor Mus musculus 116-125 1716490-1 1990 A major role of TNF in pulmonary fibrosis is supported by the following evidences obtained from pulmonary fibrosis induced in mice by bleomycin or silica particles; 1) these diseases are associated with a marked and lasting increase of the TNF mRNA within the lung, 2) they can be prevented by a treatment with anti TNF antibody or aggravated by a perfusion of mouse recombinant TNF, 3) an infusion of TNF-alpha can reproduce the alterations observed during pulmonary fibrosis such as growth of fibroblasts, collagen deposition, cell necrosis. Silicon Dioxide 147-153 tumor necrosis factor Mus musculus 16-19 9546746-6 1998 Persistent overexpression of both IL-1beta and TNFalpha were found at 2 and 16 weeks in the lungs of silica-exposed mice compared with air-sham control mice. Silicon Dioxide 101-107 tumor necrosis factor Mus musculus 47-55 8520788-6 1995 TNF-alpha production by BAL cells after silica exposure was significantly higher in C57BL/6J mice than in C3H/HeJ mice in the chronic phase, whereas there was no significant difference in IL-1 alpha production between both strains of silica-injected mice. Silicon Dioxide 40-46 tumor necrosis factor Mus musculus 0-9 7576690-4 1995 The level of TNF alpha production by RAW 264.7 cells increased up to 5-fold 48 h after phagocytosis of silica particles with very low cell toxicity. Silicon Dioxide 103-109 tumor necrosis factor Mus musculus 13-22 7576690-6 1995 When cells were exposed to a higher number of silica particles, cell activation was attained at shorter times but a substantial number of cells were damaged at 48 h. Interferon gamma (IFN gamma) alone induced an increased production of TNF alpha in RAW 264.7 cells, not further augmented by a subsequent exposure to silica of the IFN gamma-treated cells. Silicon Dioxide 46-52 tumor necrosis factor Mus musculus 236-245 7576690-6 1995 When cells were exposed to a higher number of silica particles, cell activation was attained at shorter times but a substantial number of cells were damaged at 48 h. Interferon gamma (IFN gamma) alone induced an increased production of TNF alpha in RAW 264.7 cells, not further augmented by a subsequent exposure to silica of the IFN gamma-treated cells. Silicon Dioxide 316-322 tumor necrosis factor Mus musculus 236-245 33844454-11 2021 Se@SiO2 nanocomposites evidently affected the reduction of pancreatic enzymes and inflammatory cytokines (IL-6, IL-1beta, TNF-alpha). Silicon Dioxide 3-7 tumor necrosis factor Mus musculus 122-131 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 49-55 tumor necrosis factor Mus musculus 18-21 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 49-55 tumor necrosis factor Mus musculus 183-186 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 49-55 tumor necrosis factor Mus musculus 183-186 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 49-55 tumor necrosis factor Mus musculus 183-186 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 18-21 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 183-186 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 183-186 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 183-186 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 18-21 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 183-186 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 183-186 2156165-4 1990 Here we show that TNF plays an important part in silica-induced pulmonary fibrosis in mice in that (1) a single instillation of silica leads to a marked increase in the level of lung TNF messenger RNA which lasts for greater than 70 days, while there are no obvious changes in the amounts of IL-1 alpha or TGF-beta mRNAs; and (2) silica-induced collagen deposition is almost completely prevented by anti-TNF antibody, but is significantly increased by continuous infusion of mouse recombinant TNF. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 183-186 2753523-11 1989 TNF production in silica-instilled mice was similar to controls, possibly due to the presence of large numbers of neutrophils (3.3 x 10(5)/lavage) that could adsorb TNF. Silicon Dioxide 18-24 tumor necrosis factor Mus musculus 0-3 2753523-11 1989 TNF production in silica-instilled mice was similar to controls, possibly due to the presence of large numbers of neutrophils (3.3 x 10(5)/lavage) that could adsorb TNF. Silicon Dioxide 18-24 tumor necrosis factor Mus musculus 165-168 2753523-12 1989 In vitro experiments showed an augmentation of TNF production by bronchoalveolar cells in the presence of silica. Silicon Dioxide 106-112 tumor necrosis factor Mus musculus 47-50 2753523-13 1989 Taken together, our data suggest that asbestos and silica stimulate alveolar macrophages to produce TNF, which can be involved in pulmonary inflammation and fibrosis. Silicon Dioxide 51-57 tumor necrosis factor Mus musculus 100-103 32625168-10 2020 Silica challenge led to increased leukocyte numbers (mononuclear cells and neutrophils) as well as production of the chemokine KC/CXCL-1 and the cytokines TNF-alpha and TGF-beta in the bronchoalveolar lavage. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 155-164 33868442-7 2021 It also decreased the levels of TNF-alpha, IL-1beta, IL-6 in the supernatant of MH-S cells induced by SiO2, inhibited the expression of p38 MAPK, blocked the activation of NF-kappaB, and controlled the upstream inflammatory response by multiple targeting. Silicon Dioxide 102-106 tumor necrosis factor Mus musculus 32-41 32428545-6 2020 The expression levels of interleukin-6 and tumor necrosis factor-alpha in lung increased in response to silica exposure across three time points; anti-HMGB-1 could alleviate those expressions at day 28 and 84. Silicon Dioxide 104-110 tumor necrosis factor Mus musculus 43-70 32306669-0 2020 [Endoplasmic reticulum stress regulates autophagy and tumor necrosis factor-alpha secretion of RAW264.7 cells induced by silica]. Silicon Dioxide 121-127 tumor necrosis factor Mus musculus 54-81 31018046-8 2019 The level of TNF-alpha in the supernatant of SiO2 -stimulated cells gradually increased with time but decreased following melatonin administration. Silicon Dioxide 45-49 tumor necrosis factor Mus musculus 13-22 30240278-6 2019 Treatment of silica-challenged mice with anti-IL-9-neutralizing antibody inhibited lung fibrosis, as assessed by lung hydroxyproline level, and suppressed the levels of major mediators, including IL-1beta, IL-6, IL-12, CCL2, CXCL1, and TNF-alpha in BALFs. Silicon Dioxide 13-19 tumor necrosis factor Mus musculus 236-245 25388157-5 2016 The real-time PCR studies showed that (1) inhalational silica induced inflammatory responses in the heart and kidney by elevated mRNA levels of TNF-alpha, IL-6 and MCP-1; (2) early fibrotic responses in the heart were observed as elevated mRNA levels of collagen I and fibronectin. Silicon Dioxide 55-61 tumor necrosis factor Mus musculus 144-153 28138699-10 2017 Expression of IL-6 and TNF-alpha mRNA in colonic mucosa in the normal dosage, high dosage and 5-ASA-SiO2 NP group was significantly lower than that in the model group. Silicon Dioxide 100-104 tumor necrosis factor Mus musculus 23-32 28138699-11 2017 Colonic mucosal IL-6 and TNF-alpha mRNA expression in the high dosage and 5-ASA-SiO2 NP groups was significantly lower than that in the normal dosage group (P<0.05). Silicon Dioxide 80-84 tumor necrosis factor Mus musculus 25-34 22491428-5 2012 Pyrogenic silicas were remarkably more active than the precipitated one as to cytotoxicity, reactive oxygen species production, lipid peroxidation, nitric oxide synthesis, and production of tumor necrosis factor-alpha, when compared both per mass and per unit surface. Silicon Dioxide 10-17 tumor necrosis factor Mus musculus 190-217 25635824-7 2015 ELISA analysis of the supernatant of wild type and P2rx7-/- mice precision-cut lung slices showed decreased amounts of IL-6 and TNF-alpha when incubated with nano-silica. Silicon Dioxide 163-169 tumor necrosis factor Mus musculus 128-137 24053909-9 2013 A intensely pulmonary cytokines such as IL-1beta, TNF-alpha, MCP-1 were induced by crystalline silica exposure, and partly inhibited by anti-IL-1beta. Silicon Dioxide 95-101 tumor necrosis factor Mus musculus 50-59 23002437-3 2012 Pretreatment of murine macrophages with LPS, peptidoglycan, TNF-alpha, or IFN-gamma conferred protection against subsequent damage to intracellular membranes caused by photooxidative chemistries or by phagocytosis of ground silica or silica microspheres. Silicon Dioxide 224-230 tumor necrosis factor Mus musculus 60-69 23002437-3 2012 Pretreatment of murine macrophages with LPS, peptidoglycan, TNF-alpha, or IFN-gamma conferred protection against subsequent damage to intracellular membranes caused by photooxidative chemistries or by phagocytosis of ground silica or silica microspheres. Silicon Dioxide 234-240 tumor necrosis factor Mus musculus 60-69 19426594-1 2009 AIM: To study the effects of curcumin on TNF-alpha and TGF-beta1 in serum and lung tissue of SiO2-induced fibrosis in mice. Silicon Dioxide 93-97 tumor necrosis factor Mus musculus 41-50 20490462-9 2010 Th1 (IL-1beta and TNF-alpha) cytokines are underexpressed in majority of the airways tissues of silica-exposed mice. Silicon Dioxide 96-102 tumor necrosis factor Mus musculus 18-27 21033154-5 2010 Moreover, murine macrophages expressing wild type or mutated TLR4 were also treated with silica to verify the effect of TLR4 in silica-induced TNFalpha release. Silicon Dioxide 128-134 tumor necrosis factor Mus musculus 143-151 19426594-7 2009 CONCLUSION: Curcumin can decrease the level of TNF-alpha and TGF-beta1 in serum and lung tissue of SiO2-induced fibrosis in mice and have the anti-fibrosis role by deregulating cytokine level. Silicon Dioxide 99-103 tumor necrosis factor Mus musculus 47-56 19778233-0 2009 Silica-induced TNF-alpha and TGF-beta1 expression in RAW264.7 cells are dependent on Src-ERK/AP-1 pathways. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 15-24 19778233-2 2009 The aim of the present study was to investigate the roles of Src-mitogen-activated protein kinase (MAPKs)/activator protein-1 (AP-1) signaling pathways in silica-induced TNF-alpha and TGF-beta1 expression in macrophage cells (RAW264.7). Silicon Dioxide 155-161 tumor necrosis factor Mus musculus 170-179 19778233-4 2009 The induction of TNF-alpha and TGF-beta1 by silica was suppressed by Src inhibitor (PP1), ERK inhibitor (PD98059), but not by p38 kinase inhibitor (SB203580). Silicon Dioxide 44-50 tumor necrosis factor Mus musculus 17-26 19778233-7 2009 Based on these findings, it was conclude that Src-ERK/AP-1 signaling pathways are involved in the TNF-alpha and TGF-beta1 expression induced by silica in macrophages. Silicon Dioxide 144-150 tumor necrosis factor Mus musculus 98-107 18302884-1 2008 OBJECTIVE: To study the role of activator protein-1 (AP-1) in the up-regulation expression of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1(TGF-beta(1)) in silica-stimulated macrophage cells (RAW264.7). Silicon Dioxide 187-193 tumor necrosis factor Mus musculus 94-121 18302884-1 2008 OBJECTIVE: To study the role of activator protein-1 (AP-1) in the up-regulation expression of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1(TGF-beta(1)) in silica-stimulated macrophage cells (RAW264.7). Silicon Dioxide 187-193 tumor necrosis factor Mus musculus 123-132 18302884-7 2008 In 20 micromol/L Curcumin prevention group and silica stimulated group, the expression of TNF-alpha protein were 23.58 +/- 45.78 and 32.12 +/- 5.34, and the expression of TGF-beta(1) protein were 1582.18 +/- 437.52 and 55.60 +/- 5.51 (P < 0.05 =; the expression of TNF-alpha, TGF-beta(1) mRNA were 0.74 +/- 0.01, 0.22 +/- 0.04 and 2.27 +/- 0.33, 2.96 +/- 0.15 (P < 0.05 =. Silicon Dioxide 47-53 tumor necrosis factor Mus musculus 90-99 18302884-7 2008 In 20 micromol/L Curcumin prevention group and silica stimulated group, the expression of TNF-alpha protein were 23.58 +/- 45.78 and 32.12 +/- 5.34, and the expression of TGF-beta(1) protein were 1582.18 +/- 437.52 and 55.60 +/- 5.51 (P < 0.05 =; the expression of TNF-alpha, TGF-beta(1) mRNA were 0.74 +/- 0.01, 0.22 +/- 0.04 and 2.27 +/- 0.33, 2.96 +/- 0.15 (P < 0.05 =. Silicon Dioxide 47-53 tumor necrosis factor Mus musculus 268-277 18302884-8 2008 CONCLUSION: The expression of TNF-alpha, TGF-beta(1) mRNA and proteins is associated with activation of AP-1 in silica-stimulated macrophage cells. Silicon Dioxide 112-118 tumor necrosis factor Mus musculus 30-39 16902192-8 2007 However, TNF-alpha, IL-13, monocyte chemotactic protein-1, protease activity, and production of ROS were dose-dependently increased after silica exposure, and production was enhanced after Fc epsilon RI stimulation. Silicon Dioxide 138-144 tumor necrosis factor Mus musculus 9-18 16902192-11 2007 Silica-induced ROS formation, apoptosis, and TNF-alpha production were reduced in BMMC obtained from SR-A, MARCO, and SR-A/MARCO knockout mice. Silicon Dioxide 0-6 tumor necrosis factor Mus musculus 45-54